拉明
核板
少突胶质细胞
生物
LMNA公司
小胶质细胞
体细胞
细胞生物学
祖细胞
神经干细胞
干细胞
分子生物学
基因
遗传学
核蛋白
核心
中枢神经系统
神经科学
免疫学
髓鞘
炎症
转录因子
作者
Yasuharu Takamori,Yukie Hirahara,Taku Wakabayashi,Tetsuji Mori,Taro Koike,Yosky Kataoka,Yasuhisa Tamura,Shuji Kurebayashi,Kiyoshi Kurokawa,Hisao Yamada
出处
期刊:IBRO Reports
[Elsevier]
日期:2018-12-01
卷期号:5: 99-109
被引量:14
标识
DOI:10.1016/j.ibror.2018.11.001
摘要
Lamins are type V intermediate filament proteins that are located beneath the inner nuclear membrane. In mammalian somatic cells, LMNB1 and LMNB2 encode somatic lamins B1 and B2, respectively, and the LMNA gene is alternatively spliced to generate somatic lamins A and C. Mutations in lamin genes have been linked to many human hereditary diseases, including neurodegenerative disorders. Knowledge about lamins in the nervous system has been accumulated recently, but a precise analysis of lamin subtypes in glial cells has not yet been reported. In this study we investigated the composition of lamin subtypes in neurons, astrocytes, oligodendrocyte-lineage cells, and microglia in the adult rat cerebral cortex using an immunohistochemical staining method. Lamin A was not observed in neurons and glial cells. Lamin C was observed in astrocytes, mature oligodendrocytes and neurons, but not observed in oligodendrocyte progenitor cells. Microglia also did not stain positive for lamin C which differed from macrophages, with lamin C positive. Lamin B1 and B2 were observed in all glial cells and neurons. Lamin B1 was intensely positive in oligodendrocyte progenitor cells compared with other glial cells and neurons. Lamin B2 was weakly positive in all glial cells compared to neurons. Our current study might provide useful information to reveal how the onset mechanisms of human neurodegenerative diseases are associated with mutations in genes for nuclear lamin proteins.
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